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Mechanisms underlying short‐term modulation of transmitter release by presynaptic depolarization
Author(s) -
Hori Tetsuya,
Takahashi Tomoyuki
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.168765
Subject(s) - depolarization , postsynaptic potential , neuroscience , biophysics , egta , neurotransmission , inhibitory postsynaptic potential , neural facilitation , chemistry , facilitation , excitatory postsynaptic potential , biology , calcium , biochemistry , receptor , organic chemistry
Presynaptic terminal depolarization modulates the efficacy of transmitter release. Residual Ca 2+ remaining after presynaptic depolarization is thought to play a critical role in facilitation of transmitter release, but its downstream mechanism remains unclear. By making simultaneous pre‐ and postsynaptic recordings at the rodent calyx of Held synapse, we have investigated mechanisms involved in the facilitation and depression of postsynaptic currents induced by presynaptic depolarization. In voltage‐clamp experiments, cancellation of the Ca 2+ ‐dependent presynaptic Ca 2+ current ( I pCa ) facilitation revealed that this mechanism can account for 50% of postsynaptic current facilitation, irrespective of intraterminal EGTA concentrations. Intraterminal EGTA, loaded at 10 m m , failed to block postsynaptic current facilitation, but additional BAPTA at 1 m m abolished it. Potassium‐induced sustained depolarization of non‐dialysed presynaptic terminals caused a facilitation of postsynaptic currents, superimposed on a depression, with the latter resulting from reductions in presynaptic action potential amplitude and number of releasable vesicles. We conclude that presynaptic depolarization bidirectionally modulates transmitter release, and that the residual Ca 2+ mechanism for synaptic facilitation operates in the immediate vicinity of voltage‐gated Ca 2+ channels in the nerve terminal.